Anesthesiology
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Detection and hemodynamic consequences of venous air embolism. Does nitrous oxide make a difference?
Volume expansion of intravascular air by nitrous oxide (N2O) may improve the sensitivity of monitors used to detect venous air embolism (VAE) and/or exacerbate hemodynamic changes following VAE. The purpose of this study was to determine if the administration of N2O alters the sensitivity (i.e., threshold of detection) of monitors used to detect VAE or the hemodynamic consequences of VAE. Twenty-one dogs were monitored for VAE with precordial Doppler ultrasound, transesophageal echocardiography (TEE), changes in end-tidal carbon dioxide tension (ETCO2), and changes in pulmonary artery pressure (PAP). ⋯ Positive responses were defined as follows: unmistakable audible change in frequency on Doppler ultrasound, visualization of densities consistent with air bubbles in the right cardiac chambers or outflow tract on TEE, a decrease in ETCO2 greater than or equal to 2 mmHg, and an increase in mean PAP greater than or equal to 3 mmHg. In group 3 (n = 7), venous air was infused at rates between 0.1 and 0.8 ml.kg-1.min-1 during 1 MAC (total anesthetic level) of isoflurane with and without 50% N2O. In group 3, N2O administration was discontinued immediately upon Doppler detection of VAE and air infusion continued until mean arterial pressure (MAP) decreased by 10 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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Randomized Controlled Trial Clinical Trial
Effects of bolus administration of ORG-9426 in children during nitrous oxide-halothane anesthesia.
ORG-9426 is a new steroidal nondepolarizing neuromuscular blocking drug. We determined the dose-response relationship of ORG-9426 in 62 children (aged 1-5 yr) during nitrous oxide-halothane anesthesia by means of log-probit transformation and least-squares linear regression of the initial dose and response. Twelve additional patients received a bolus of 600 micrograms/kg (2 X the dose estimated to produce 95% depression of neuromuscular function [ED95]) of ORG-9426. ⋯ Time from administration of 600 micrograms/kg to onset of 90% and 100% neuromuscular block was 0.8 +/- 0.1 (0.5-1.3) and 1.3 +/- 0.2 (0.7-2.8) min. The time to recovery of neuromuscular transmission to 25% (T25) was 26.7 +/- 1.9 (17.2-39.0) min. The recovery index (T25-75) was 11.0 +/- 1.6 (6.0-22.8) min, and the time to complete recovery of the magnitude of the fourth response to a train-of-four stimuli divided by the magnitude of the first response (T4/T1) greater than or equal to 0.75 was 41.9 +/- 3.2 (26.5-57.7) min.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical Trial Controlled Clinical Trial
Ventilatory effects of clonidine alone and in the presence of alfentanil, in human volunteers.
Clonidine, an alpha 2-adrenergic agonist, can potentiate opioid-induced analgesia. In a double-blind placebo-controlled study in human volunteers, we sought to determine whether clonidine also potentiates opioid-induced respiratory depression. Hypercapnic ventilatory responses (minute ventilation, mean inspiratory flow rate, and mouth occlusion pressure) were measured in five healthy male volunteers on two separate occasions (with or without clonidine, approximately 3.5 micrograms.kg-1 orally) under the following conditions: baseline, 2 h after clonidine/placebo (alfentanil concentration of 0), and during computer-controlled alfentanil infusions to approximate plasma concentrations of 5, 10, 20, 40, and 80 ng.ml-1. ⋯ The mouth occlusion pressure was not affected by clonidine treatment. Clonidine treatment did not potentiate alfentanil-induced respiratory depression. Although the combination of an opioid and an alpha 2-adrenergic agonist may act synergistically for the analgesic response, there is no synergistic effect by this drug combination on respiratory depression.
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We prospectively studied 952 patients to identify the incidence of hypotension (systolic blood pressure less than 90 mmHg), bradycardia (heart rate less than 50 beats/min), nausea, vomiting, and dysrhythmia during spinal anesthesia. Historical, clinical, and physiologic data were correlated with the incidence of these side effects by univariate and multivariate analysis. Hypotension developed in 314 patients (33%), bradycardia in 125 (13%), nausea in 175 (18%), vomiting in 65 (7%), and dysrhythmia in 20 (2%). ⋯ Variables conferring increased odds of developing bradycardia include a baseline heart rate less than 60 beats/min (odds ratio 4.9, P less than 0.001), ASA physical status classification of 1 versus 3 or 4 (3.5, P less than 0.001), current therapy with beta-adrenergic blocking drugs (2.9, P less than 0.001), and peak block height greater than or equal to T5 (1.7, P = 0.02). Variables conferring increased odds of developing nausea or vomiting include addition of phenylephrine or epinephrine to the local anesthetic (3.0-6.3, P less than or equal to 0.003), peak block height greater than or equal to T5 (odds ratio 3.9, P less than 0.001), use of procaine (2.6-4.4, P less than or equal to 0.003), baseline heart rate greater than or equal to 60 beats/min (2.3, P = 0.03), history of carsickness (2.0, P = 0.01), and development of hypotension during spinal anesthesia (1.7, P = 0.009). Our results indicate that the incidence of side effects during spinal anesthesia may be reduced by 1) minimizing peak block height; 2) using plain solutions of local anesthetics; 3) performing the spinal puncture at or below the L3-L4 interspace; and 4) avoiding the use of procaine in the subarachnoid space.
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We investigated the feasibility of performing thoracic epidural anesthesia via the caudal approach in 20 children (age 62 +/- 38 months and weight 18.5 +/- 7.3 kg; mean +/- standard deviation). Based on external landmarks, a predetermined length of 24-G epidural catheter (Concord Portex 20/24 microcatheter system) with stylet was passed into the epidural space through a 20-G intravenous catheter inserted through the sacrococcygeal ligament, and a radiograph of the abdomen and chest was obtained. The radiographically determined catheter tip position was within two vertebrae of the target position in 17 of 20 subjects. ⋯ Intraoperative caudal anesthesia and postoperative pain relief were satisfactory in all 20 subjects. We have found it possible to use the caudal approach to thoracic epidural anesthesia in children as old as 10 yr. Ease of removal of the stylet, ease of injection, and negative aspiration and test doses predict successful placement and obviate the need for routine radiographic confirmation of catheter position.